ArticleAutophagy2024
CKLF induces microglial activation via triggering defective mitophagy and mitochondrial dysfunction.
Article in Autophagy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
What it found
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The trial behind it
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Who cites it
56 citing papers in PubMed, 72 citations in OpenAlex.
- 3C suppresses PINK1-mediated mitophagy and contributes to coxsackievirus B3 replication.Virulence · 2026Article
- Mechanisms and therapeutic potential of mitochondrial-targeted therapies in bone repair.Annals of medicine · 2026Review
- Nanomaterial-driven spatiotemporal autophagy modulation: The dual-edged sword in precision cancer therapy.Acta pharmaceutica Sinica. B · 2026Review
- Entorhinal Astrocyte Transplants Restore Spatial Exploration and Alleviate Amyloid-Beta Pathology in Alzheimer's Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Microglial Immunometabolic Remodeling After Ischemic Stroke: The Interplay Between Mitochondrial Stress and the Ischemic Microenvironment.Translational stroke research · 2026Review
- Exercise as a Molecular Therapeutic Strategy in Metabolic Syndrome: Integrating Cellular Signaling, Organ Crosstalk, and Clinical Translation-A Narrative Review.Current issues in molecular biology · 2026Review
- Multi-omics analysis identifies CKLF as a promoter for HCC progression by regulating the AKT, ERK pathways, and infiltrating immune cells.Translational oncology · 2026Article
- Aldose reductase inhibition suppresses microglial endoplasmic reticulum stress and ferritinophagy in ischemic stroke.Acta pharmacologica Sinica · 2026Article
- Extracellular Mitochondria Mediate Endothelial Injury After Traumatic Brain Injury.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Temporin-GHaR6R Peptide Ameliorates Experimental Autoimmune Encephalomyelitis by Suppressing Microglial M1 Polarization and Mitochondrial Dynamics Dysfunction.Probiotics and antimicrobial proteins · 2026Article
- Microglial mitophagy as an immunometabolic checkpoint in alzheimer's disease: linking mitochondrial quality control to neuroinflammation.Journal of neuroinflammation · 2026Review
- Hydrogen alleviates sepsis-associated encephalopathy via ATG9B-dependent mitophagy.Molecular medicine (Cambridge, Mass.) · 2026Article
- Nrf2 Activators in Parkinson's Disease: Modulating Mitophagy and Regulating Cuproptosis.Molecular neurobiology · 2026Review
- Restoration of macrophage mitochondrial dynamics and trafficking with enzymatic magnesium-manganese layered double hydroxide for osteoporotic therapy.Journal of nanobiotechnology · 2026Article
- PYGL-driven glycogenolysis impairs microglial autophagic fluxActa pharmaceutica Sinica. B · 2026Article
- Microglial Mitochondrial Dysfunction: The Storm Center of Post-Stroke Neuroinflammation.CNS neuroscience & therapeutics · 2026Review
- Microglial IRF7-induced lipophagy impairment aggravates lipid droplet overload and impedes neurological recovery after ischemic stroke.Journal of neuroinflammation · 2026Article
- Ginsenoside Rg1 alleviates post-ischemic stroke neuroinflammation by inhibiting CKLF1-mediated suppression of dead/dying neuron clearance.Acta pharmaceutica Sinica. B · 2026Article
- Article
- A neutrophil-intrinsic CKLF1-PKM2 axis drives glycolytic flux for de novo DAG synthesis and pro-inflammatory ROS production.Cell death and differentiation · 2026Article
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although microglial activation is induced by an increase in chemokines, the role of mitophagy in this process remains unclear. This study aimed to elucidate the role of microglial mitophagy in CKLF/CKLF1 (chemokine-like factor 1)-induced microglial activation and neuroinflammation, as well as the underlying molecular mechanisms following CKLF treatment. This study determined that CKLF, an inducible chemokine in the brain, leads to an increase in mitophagy markers, such as DNM1L, PINK1 (PTEN induced putative kinase 1), PRKN, and OPTN, along with a simultaneous increase in autophagosome formation, as evidenced by elevated levels of BECN1 and MAP1LC3B (microtubule-associated protein 1 light chain 3 beta)-II. However, SQSTM1, a substrate of autophagy, was also accumulated by CKLF treatment, suggesting that mitophagy flux was reduced and mitophagosomes accumulated. These findings were confirmed by transmission electron microscopy and confocal microscopy. The defective mitophagy observed in our study was caused by impaired lysosomal function, including mitophagosome-lysosome fusion, lysosome generation, and acidification, resulting in the accumulation of damaged mitochondria in microglial cells. Further analysis revealed that pharmacological blocking or gene-silencing of mitophagy inhibited CKLF-mediated microglial activation, as evidenced by the expression of the microglial marker AIF1 (allograft inflammatory factor 1) and the mRNA of proinflammatory cytokines (
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.